The cortical sleep slow oscillation is attributed a role in memory consolidation. It has been shown to reveal a tight temporal correlation to brain electric events such as sleep spindles and sharp wave ripples, with these events occurring predominantly at a specific phase of the cortical slow oscillation. Boosting the sleep slow oscillation by oscillatory weak electric currents in humans and rats during non-rapid eye movement (NREM) sleep has improved memory performance, and enhanced dominant NREM sleep rhythms. Hippocampal reactivation is one mechanism of neurons and local neuronal networks through which post-experience information processing can occur. Here we aim firstly, to identify the causal contribution of neurons and oscillatory networks in hippocampus and prefrontal cortex to sleep-dependent memory consolidation in behaving mice. The causal effect of optogenetically silencing i) of hippocampal CA1 output on memory consolidation and on prefrontocortical (PFC) activity and ii) of prefrontocortical neurons on memory consolidation and on hippocampal activity are to be investigated. Moreover, we investigate in parallel the causal bi-directional relationship between the sleep slow oscillation and neuronal ensemble activity in hippocampus and mPFC by manipulating the slow oscillatory field during NREM sleep. To fulfill these aims we develop and combine usage of optogenetics, high density multi-electrode recordings, hippocampus-dependent tasks closely comparable to tasks used in human subjects. Furthermore we construct a customized stimulator to produce endogenous pattern-based waveforms and stimulate utilizing information derived from finite element modelling of the mouse brain. Advanced analyses will furthermore enable the detection of real-time interactions between the investigated brain regions.